P53 PROTEIN EXPRESSION IN LYMPHOMAS AND REACTIVE LYMPHOID-TISSUE

Citation
R. Villuendas et al., P53 PROTEIN EXPRESSION IN LYMPHOMAS AND REACTIVE LYMPHOID-TISSUE, Journal of pathology, 166(3), 1992, pp. 235-241
Citations number
25
Journal title
ISSN journal
00223417
Volume
166
Issue
3
Year of publication
1992
Pages
235 - 241
Database
ISI
SICI code
0022-3417(1992)166:3<235:PPEILA>2.0.ZU;2-E
Abstract
P53 is a tumour suppressor gene, located in the short arm of chromosom e 17, which encodes for a nuclear protein involved in the control of c ellular growth, regulating the entry of the cell into the S-phase. P53 mutations have been identified in a progressively increasing number o f human malignancies. Nuclear p53 protein is usually present in non-tu mour cells in minute concentrations, due to its short half-life. In co ntrast, tumours with p53 mRNA mutations show a higher nuclear protein concentration, detectable by immunohistological techniques, due to sta bilization by complexing with other proteins such as heat-shock protei n or wild-type p53 protein. Levels of nuclear p53 protein detected by immunohistochemistry with the monoclonal antibody PAb 1801 were measur ed with the aid of an image analysis system in 83 non-Hodgkin's lympho mas (NHLs) and 13 cases of Hodgkin's disease, as well as in 14 cases o f normal thymus, reactive tonsils, and lymphadenitis. High levels of p 53 protein (> 5 per cent of the cells) were present only in high-grade lymphomas (in the proportion 13/55), with a peak incidence in Burkitt 's lymphoma (5/8 cases). Lower levels (< 5 per cent) of p53 protein we re detected in low-grade B- and T-cell lymphomas, as well as in most o f the cases of Hodgkin's disease, where p53 protein was selectively pr esent in Hodgkin and Reed-Sternberg cells. In 5/14 reactive tonsils or lymph nodes, occasional p53-positive cells were identified. These res ults suggest a relationship between levels of p53 protein and the aggr essiveness of NHL. The sporadic presence of p53-positive cells in huma n reactive tissues suggests that its expression could depend not only on mutation, but also on stabilization of the protein through complexi ng with other nuclear proteins. It is not known if this mechanism is a lso responsible for the p53 nuclear accumulation in high-grade lymphom as.